Fuchs, Eberhard

[["dc.bibliographiccitation.firstpage","97"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","106"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Schneider, E."],["dc.contributor.author","Jensen, L. R."],["dc.contributor.author","Farcas, R."],["dc.contributor.author","Kondova, I."],["dc.contributor.author","Bontrop, R. E."],["dc.contributor.author","Navarro, B."],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Kuss, A. W."],["dc.contributor.author","Haaf, T."],["dc.date.accessioned","2019-07-09T11:54:38Z"],["dc.date.available","2019-07-09T11:54:38Z"],["dc.date.issued","2012"],["dc.description.abstract","The human brain is distinguished by its remarkable size, high energy consumption, and cognitive abilities compared to all other mammals and non-human primates. However, little is known about what has accelerated brain evolution in the human lineage. One possible explanation is that the appearance of advanced communication skills and language has been a driving force of human brain development. The phenotypic adaptations in brain structure and function which occurred on the way to modern humans may be associated with specific molecular signatures in today’s human genome and/or transcriptome. Genes that have been linked to language, reading, and/or autism spectrum disorders are prime candidates when searching for genes for human-specific communication abilities. The database and genome-wide expression analyses we present here revealed a clustering of such communication-associated genes (COAG) on human chromosomes X and 7, in particular chromosome 7q31-q36. Compared to the rest of the genome, we found a high number of COAG to be differentially expressed in the cortices of humans and non-human primates (chimpanzee, baboon, and/or marmoset). The role of X-linked genes for the development of human-specific cognitive abilities is well known. We now propose that chromosome 7q31-q36 also represents a hot spot for the evolution of human-specific communication abilities. Selective pressure on the T cell receptor beta locus on chromosome 7q34, which plays a pivotal role in the immune system, could have led to rapid dissemination of positive gene variants in hitchhiking COAG."],["dc.format.extent","10"],["dc.identifier.doi","10.1159/000335465"],["dc.identifier.fs","593150"],["dc.identifier.pmid","22261840"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60698"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1424-859X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A High Density of Human Communication-Associated Genes in Chromosome 7q31-q36: Differential Expression in Human and Non-Human Primate Cortices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","278"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","287"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Schneider, E."],["dc.contributor.author","Mayer, S."],["dc.contributor.author","El Hajj, N."],["dc.contributor.author","Jensen, L. R."],["dc.contributor.author","Kuss, A. W."],["dc.contributor.author","Zischler, H."],["dc.contributor.author","Kondova, I."],["dc.contributor.author","Bontrop, R. E."],["dc.contributor.author","Navarro, B."],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Zechner, U."],["dc.contributor.author","Haaf, T."],["dc.date.accessioned","2019-07-09T11:54:38Z"],["dc.date.available","2019-07-09T11:54:38Z"],["dc.date.issued","2012-03-24"],["dc.description.abstract","The autism susceptibility locus on human chromosome 7q32 contains the maternally imprinted MEST and the non-imprinted COPG2 and TSGA14 genes. Autism is a disorder of the ‘social brain’ that has been proposed to be due to an overbalance of paternally expressed genes. To study regulation of the 7q32 locus during anthropoid primate evolution, we analyzed the methylation and expression patterns of MEST , COPG2, and TSGA14 in human, chimpanzee, Old World monkey (baboon and rhesus macaque), and New World monkey (marmoset) cortices. In all human and anthropoid primate cortices, the MEST promoter was hemimethylated, as expected for a differentially methylated imprinting control region, whereas the COPG2 and TSGA14 promoters were completely demethylated, typical for transcriptionally active non-imprinted genes. The MEST gene also showed comparable mRNA expression levels in all analyzed species. In contrast, COPG2 expression was downregulated in the human cortex compared to chimpanzee, Old and New World monkeys. TSGA14 either showed no differential regulation in the human brain compared to chimpanzee and marmoset or a slight upregulation compared to baboon. The human-specific downregulation supports a role for COPG2 in the development of a ‘social brain’. Promoter methylation patterns appear to be more stable during evolution than gene expression patterns, suggesting that other mechanisms may be more important for inter-primate differences in gene expression."],["dc.identifier.doi","10.1159/000337298"],["dc.identifier.fs","593149"],["dc.identifier.pmid","22456293"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9487"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60697"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1424-859X"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Methylation and Expression Analyses of the 7q Autism Susceptibility Locus Genes MEST, COPG2, and TSGA14 in Human and Anthropoid Primate Cortices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]